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The neurons of the retina, like those in the rest of the nervous system, are extremely susceptible to hypoxia.

Central retinal artery occlusions may follow thrombosis of the retinal artery, as in atherosclerosis or giant cell arteritis, or emboli of various types. Intracellular edema, manifested by retinal pallor, is prominent, especially in the macula where the ganglion cells are most numerous.

The vacularized choroid beneath the center of the macula (foveola) stands out in sharp contrast as a prominent “cherry red spot”.

The lack of retinal circulation reduces the retinal arterioles to delicate threads.

Permanent blindness follows central retinal artery obstruction, unless the ischemia is of short duration.

Unilateral blurred vision, lasting a few minutes (amaurosis fugax), occurs with small retinal emboli.

Hemorrhage is not a feature, inasmuch as the blood is not under increased pressure and simply drains away.

Visit:Normal histology and diseases of the retina ; Retinal Occlusovascular Disease ; Central Retinal Vein Occlusion ; Comparison between central retinal vein and central retinal artery occlusions ; Hypertensive Retinopathy.

           

Fundus changes in central retinal artery occlusion.Retina. 2007 Mar;27(3):276-89.

PURPOSE: To investigate systematically the ophthalmoscopic fundus findings associated with central retinal artery occlusion (CRAO). METHODS: The study included 240 consecutive patients (248 eyes) with CRAO. The eyes underwent detailed fundus evaluation and stereoscopic color fundus photography at initial and follow-up visits. Patients without evidence of giant cell arteritis were advised to have carotid Doppler imaging and echocardiography to determine the source of emboli. CRAO was classified into 3 types: permanent CRAO (175 eyes), permanent CRAO with cilioretinal artery sparing (35 eyes), and transient CRAO (38 eyes). In the three types of CRAO, acute-phase and late-phase changes in the retina, optic disk, and retinal vessels were evaluated. RESULTS: The main findings during the initial examination in our clinic for permanent CRAO were retinal opacity in the posterior pole (58%), cherry-red spot (90%), box-carring (19%), retinal arterial attenuation (32%), and optic disk edema (22%) and pallor (39%). The most frequent findings identified at the late stage, based on survivorship curves, were optic atrophy (91%), retinal arterial attenuation (58%), cilioretinal collaterals (18%), and macular retinal pigment epithelial changes (11%). Compared with permanent CRAO, permanent CRAO with cilioretinal artery sparing was associated with a lower incidence of all macular and optic disk abnormalities. For transient CRAO, the incidence of initial findings varied greatly compared with the other types. Intraarterial emboli were observed in 20% of patients. Carotid Doppler evaluation identified carotid vascular plaques in 67% of patients tested and hemodynamically significant (>50%) obstruction in 32%. Four percent of CRAOs presented with simultaneous bilateral onset. CONCLUSIONS: The type and incidence of fundus findings at the initial visit and in the late phase of CRAO vary by its type. This study confirms that retinal opacity is predominantly evident in the posterior retina, that optic disk findings at presentation are common, that CRAO associated with normal-appearing retinal vessels and/or optic disk is not rare, and that observation of emboli is infrequent. Clinicians should be aware of the various presentation findings during the acute and late stages of CRAO and its various types. A complete picture of CRAO is provided by combined information of our clinical and experimental studies of CRAO.

Central retinal artery occlusion: findings in optical coherence tomography and functional correlations. Eur J Med Res. 2006 Jun 30;11(6):250-2.

BACKGROUND: Visual prognosis in central retinal artery occlusion (CRAO) is poor and not predictable in individual patients. There may be a correlation between visual acuity and extent of initial macular edema. METHODS: Central retinal thickness of eleven patients with subtotal CRAO was measured with optical coherence tomography (OCT). Patients' acute-stage macular thicknesses were compared to those of later stages. Values are given as mean (+/-standard error; range). RESULTS: The mean age of the eleven patients was 68.8 years (62-75). Eight men and three women were examined. The mean initial duration of CRAO was 24.7 (+/- 5.0; 4-77) hours. Initial central thickness was 372.5 (+/- 27.1; 258-522) microm. After 5.7 (+/- 1.5; 1-17) months, mean reduction in macular edema was 197 (+/- 31.3; 63-391) microm. Visual acuity (VA) improved from 0.0125 (+/- 0.2; blindness -0.6) to 0.035 (+/- 0.2; blindness - 0.8) namely 4.5 lines. This difference was significant (p= 0.023). 6/11 patients (55 %) initially had a pronounced central retinal edema (>380 microm). No correlation was found between the initial macular edema height and visual improvement. CONCLUSIONS: The extent of macular edema differs widely and does not affect visual prognosis in CRAO eyes.

Central retinal artery occlusion: visual outcome. Am J Ophthalmol. 2005 Sep;140(3):376-91.

PURPOSE: To investigate systematically the natural history of visual outcome in central retinal artery occlusion (CRAO). DESIGN: Cohort study. METHODS: At entry, 244 consecutive patients (260 eyes) with CRAO (seen consecutively from 1973 to 2000) had a detailed ocular and medical history and ocular evaluation. CRAO eyes were classified into four categories: non-arteritic (NA) CRAO (171 eyes), NA-CRAO with cilioretinal artery sparing (35), transient NA-CRAO (41), and arteritic CRAO (13). RESULTS: Within 7 days of onset of CRAO, initial visual acuity differed among the four CRAO types (P < .0001). In eyes with vision of counting fingers or worse, it improved in 82% of eyes with transient NA-CRAO, 67% of eyes with NA-CRAO with cilioretinal artery sparing, and 22% of eyes with NA-CRAO. Visual acuity improved primarily within the first 7 days (P < .0001). In the central 30-degree visual field, central scotoma was most common. Central visual field improved in 39% with transient NA-CRAO, 25% with NA-CRAO with cilioretinal artery sparing, and 21% with NA-CRAO. Peripheral visual field was normal in 62.9% of eyes with transient NA-CRAO and 22.1% in those with NA-CRAO. In 51.9% of eyes with NA-CRAO, the only remaining visual field was a peripheral island. Peripheral fields improved in NA-CRAO (39%) and in transient NA-CRAO (39%). CONCLUSIONS: Classification of CRAO is crucial for understanding differences in visual outcome. Marked improvement in visual acuity and visual field can occur without treatment and is determined by several factors. Visual field information is essential to evaluate visual disability in CRAO.

Central retinal artery occlusion. Retinal survival time. Exp Eye Res. 2004 Mar;78(3):723-36.

PURPOSE: To investigate the retinal survival time following central retinal artery occlusion (CRAO). METHODS: In 38 elderly, atherosclerotic and hypertensive rhesus monkeys, transient CRAO (varying from 97 to 240 min) was produced by temporarily clamping the CRA at its site of entry into the optic nerve. Stereoscopic color fundus photography, fluorescein fundus angiography, electroretinography (ERG), and visual evoked potential (VEP) recording were performed before and during CRA clamping, after unclamping, and serially thereafter. After unclamping of the CRA, the animals were followed for variable lengths of time (median duration 8.14 weeks). Finally, the eyes and optic nerves were examined histologically. The data on ERG changes were analyzed in the following four time frames: (1) baseline before CRA clamping, (2) during CRA clamping, (3) immediately after unclamping, and (4) at the end of follow-up. Duration of CRAO was divided into four groups: 97, 105-120, 150-165, and > or = 180 min. RESULTS: A 'negative ERG' appeared during CRA clamping. With removal of the CRA clamp, there was b-wave recovery, with differential rates of recovery of ERG-eyes with shorter CRAO recovered sooner than those with longer occlusion. On removal of clamp, recovery was seen in scotopic 24 dB b-wave, photopic 0 dB single flash b-wave and 30 Hz flicker, with the b/a ratio of the combined rod and cone response and selective rod response showing statistically significant differences amongst the shorter and longer periods of CRAO. A delayed normalization of the depressed b/a ratio immediately after CRA reperfusion may indicate high-grade ischemic damage. At the final follow-up test session, no clear-cut derangement of any ERG parameter was seen for any group, with subtotal b-wave amplitude recovery for all groups. Longer CRAO produced incomplete VEP recovery. On histology, in the macular retina, eyes with CRAO for 97 min showed practically no damage, but duration of CRAO was found to be significantly associated with the amount of damage in the ganglion cell layer (p = 0.009) and inner nuclear layer (p = 0.017). Outer nuclear and plexiform layers and photoreceptors showed no damage at all with CRAO. There was no significant association of the ERG measures and histologic changes with any of the residual retinal circulation variables. CONCLUSIONS: Our electrophysiologic, histopathologic and morphometric studies showed that the retina of old, atherosclerotic, hypertensive rhesus monkeys suffers no detectable damage with CRAO of 97 min but above that level, the longer the CRAO, the more extensive the irreversible damage. The study suggests that CRAO lasting for about 240 min results in massive irreversible retinal damage.

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